scholarly journals Role of Streptococcus pyogenes Two-Component Response Regulators in the Temporal Control of Mga and the Mga-Regulated Virulence Gene emm

2004 ◽  
Vol 72 (6) ◽  
pp. 3668-3673 ◽  
Author(s):  
Deborah A. Ribardo ◽  
Thomas J. Lambert ◽  
Kevin S. McIver
Keyword(s):  
Streptococcus Pyogenes ◽  
Virulence Genes ◽  
Stationary Phases ◽  
Virulence Gene ◽  
Temporal Control ◽  
Wild Type ◽  
Response Regulators ◽  
Two Component

ABSTRACT We examined the role of Streptococcus pyogenes two-component response regulators (SptR) in expression of Mga and the Mga-regulated gene emm. Both serotype M6 and serotype M1 mutants in 12 of the 13 identified sptR genes exhibited levels of emm transcripts and Mga protein comparable to those of the wild type during exponential and stationary phases of growth. Thus, temporal control of these virulence genes does not require Spt response regulators.

scholarly journals FixJ family regulator AcfR of Azorhizobium caulinodans is involved in symbiosis with the host plant

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Liu ◽  
Xue Bai ◽  
Yan Li ◽  
Haikun Zhang ◽  
Xiaoke Hu
Keyword(s):  
Signal Transduction ◽  
Host Plant ◽  
Type Strain ◽  
Wild Type Strain ◽  
Response Regulator ◽  
Azorhizobium Caulinodans ◽  
Wild Type ◽  
Response Regulators ◽  
Free Living ◽  
Two Component

Abstract Background A wide variety of bacterial adaptative responses to environmental conditions are mediated by signal transduction pathways. Two-component signal transduction systems are one of the predominant means used by bacteria to sense the signals of the host plant and adjust their interaction behaviour. A total of seven open reading frames have been identified as putative two-component response regulators in the gram-negative nitrogen-fixing bacteria Azorhizobium caulinodans ORS571. However, the biological functions of these response regulators in the symbiotic interactions between A. caulinodans ORS571 and the host plant Sesbania rostrata have not been elucidated to date. Results In this study, we identified and investigated a two-component response regulator, AcfR, with a phosphorylatable N-terminal REC (receiver) domain and a C-terminal HTH (helix-turn-helix) LuxR DNA-binding domain in A. caulinodans ORS571. Phylogenetic analysis showed that AcfR possessed close evolutionary relationships with NarL/FixJ family regulators. In addition, six histidine kinases containing HATPase_c and HisKA domains were predicted to interact with AcfR. Furthermore, the biological function of AcfR in free-living and symbiotic conditions was elucidated by comparing the wild-type strain and the ΔacfR mutant strain. In the free-living state, the cell motility behaviour and exopolysaccharide production of the ΔacfR mutant were significantly reduced compared to those of the wild-type strain. In the symbiotic state, the ΔacfR mutant showed a competitive nodule defect on the stems and roots of the host plant, suggesting that AcfR can provide A. caulinodans with an effective competitive ability for symbiotic nodulation. Conclusions Our results showed that AcfR, as a response regulator, regulates numerous phenotypes of A. caulinodans under the free-living conditions and in symbiosis with the host plant. The results of this study help to elucidate the involvement of a REC + HTH_LuxR two-component response regulator in the Rhizobium-host plant interaction.

scholarly journals The Regulator PerR Is Involved in Oxidative Stress Response and Iron Homeostasis and Is Necessary for Full Virulence of Streptococcus pyogenes

2002 ◽  
Vol 70 (9) ◽  
pp. 4968-4976 ◽  
Author(s):  
Susanna Ricci ◽  
Robert Janulczyk ◽  
Lars Björck
Keyword(s):  
Oxidative Stress ◽  
Streptococcus Pyogenes ◽  
Stress Responses ◽  
Metal Binding ◽  
Iron Homeostasis ◽  
Bacterial Species ◽  
Transcriptional Analysis ◽  
Wild Type ◽  
Allelic Replacement

ABSTRACT Ferric uptake regulator (Fur) and Fur-like proteins form an important family of transcriptional regulators in many bacterial species. In this work we have characterized a Fur-like protein, the peroxide regulator PerR, in an M1 serotype of Streptococcus pyogenes. To determine the role of PerR in S. pyogenes, we inactivated the gene by allelic replacement. PerR-deficient bacteria showed 48% reduction of 55Fe incorporation from the culture medium. Transcriptional analysis revealed that mtsA, encoding a metal-binding protein of an ABC transporter in S. pyogenes, was transcribed at lower levels than were wild-type cells. Although total iron accumulation was reduced, the growth of the mutant strain was not significantly hampered. The mutant showed hyperresistance to hydrogen peroxide, and this response was induced in wild-type cells by growth in aerobiosis, suggesting that PerR acts as an oxidative stress-responsive repressor. PerR may also participate in the response to superoxide stress, as the perR mutant was more sensitive to the superoxide anion and had a reduced transcription of sodA, which encodes the sole superoxide dismutase of S. pyogenes. Complementation of the mutation with a functional perR gene restored 55Fe incorporation, response to peroxide stress, and transcription of both mtsA and sodA to levels comparable to those of wild-type bacteria. Finally, the perR mutant was attenuated in virulence in a murine air sac model of infection (P < 0.05). These results demonstrate that PerR is involved in the regulation of iron homeostasis and oxidative stress responses and that it contributes to the virulence of S. pyogenes.

Role of the N-terminal region and of β-sheet residue Thr29 on the activity of the ω2 global regulator from the broad-host range Streptococcus pyogenes plasmid pSM19035

2005 ◽  
Vol 386 (9) ◽  
Author(s):  
Karin Welfle ◽  
Florencia Pratto ◽  
Rolf Misselwitz ◽  
Joachim Behlke ◽  
Juan C. Alonso ◽  
...  
Keyword(s):  
Host Range ◽  
Streptococcus Pyogenes ◽  
Regulatory Protein ◽  
Terminal Region ◽  
Broad Host Range ◽  
Wild Type ◽  
Global Regulator ◽  
Β Sheet

AbstractThe dimeric regulatory protein wild-type ω (wt ω

scholarly journals The bvr Locus of Listeria monocytogenes Mediates Virulence Gene Repression by β-Glucosides

1999 ◽  
Vol 181 (16) ◽  
pp. 5024-5032 ◽  
Author(s):  
Klaus Brehm ◽  
María-Teresa Ripio ◽  
Jürgen Kreft ◽  
José-Antonio Vázquez-Boland
Keyword(s):  
Listeria Monocytogenes ◽  
Virulence Genes ◽  
Natural Habitat ◽  
Sensory System ◽  
Virulence Gene ◽  
Gene Repression ◽  
Signal Molecules ◽  
Wild Type ◽  
Phosphotransferase System ◽  
Virulence Gene Expression

ABSTRACT The β-glucoside cellobiose has been reported to specifically repress the PrfA-dependent virulence genes hly andplcA in Listeria monocytogenes NCTC 7973. This led to the hypothesis that β-glucosides, sugars of plant origin, may act as signal molecules, preventing the expression of virulence genes if L. monocytogenes is living in its natural habitat (soil). In three other laboratory strains (EGD, L028, and 10403S), however, the effect of cellobiose was not unique, and all fermentable carbohydrates repressed hly. This suggested that the downregulation of virulence genes by β-glucosides is not a specific phenomenon but, rather, an aspect of a global regulatory mechanism of catabolite repression (CR). We assessed the effect of carbohydrates on virulence gene expression in a panel of wild-type isolates of L. monocytogenes by using the PrfA-dependent phospholipase C geneplcB as a reporter. Utilization of any fermentable sugar caused plcB repression in wild-type L. monocytogenes. However, an EGD variant was identified in which, as in NCTC 7973, plcB was only repressed by β-glucosides. Thus, the regulation of L. monocytogenes virulence genes by sugars appears to be mediated by two separate mechanisms, one presumably involving a CR pathway and another specifically responding to β-glucosides. We have identified in L. monocytogenes a 4-kb operon, bvrABC, encoding an antiterminator of the BglG family (bvrA), a β-glucoside-specific enzyme II permease component of the phosphoenolpyruvate-sugar phosphotransferase system (bvrB), and a putative ADP-ribosylglycohydrolase (bvrC). Low-stringency Southern blots showed that this locus is absent from other Listeria spp. Transcription ofbvrB was induced by cellobiose and salicin but not by arbutin. Disruption of the bvr operon by replacing part ofbvrAB with an interposon abolished the repression by cellobiose and salicin but not that by arbutin. Our data indicate that the bvr locus encodes a β-glucoside-specific sensor that mediates virulence gene repression upon detection of cellobiose and salicin. Bvr is the first sensory system found in L. monocytogenes that is involved in environmental regulation of virulence genes.

scholarly journals A Novel Virulence Gene in Klebsiella pneumoniae Strains Causing Primary Liver Abscess and Septic Metastatic Complications

2004 ◽  
Vol 199 (5) ◽  
pp. 697-705 ◽  
Author(s):  
Chi-Tai Fang ◽  
Yi-Ping Chuang ◽  
Chia-Tung Shun ◽  
Shan-Chwen Chang ◽  
Jin-Town Wang
Keyword(s):  
Infectious Disease ◽  
Klebsiella Pneumoniae ◽  
Liver Abscess ◽  
Virulence Genes ◽  
Wild Type Strain ◽  
Virulence Gene ◽  
Emerging Infectious Disease ◽  
High Serum ◽  
Bacterial Virulence ◽  
Wild Type

Primary Klebsiella pneumoniae liver abscess complicated with metastatic meningitis or endophthalmitis is a globally emerging infectious disease. Its pathogenic mechanism remains unclear. The bacterial virulence factors were explored by comparing clinical isolates. Differences in mucoviscosity were observed between strains that caused primary liver abscess (invasive) and those that did not (noninvasive). Hypermucoviscosity correlated with a high serum resistance and was more prevalent in invasive strains (52/53 vs. 9/52; P &lt; 0.0001). Transposon mutagenesis identified candidate virulence genes. A novel 1.2-kb locus, magA, which encoded a 43-kD outer membrane protein, was significantly more prevalent in invasive strains (52/53 vs. 14/52; P &lt; 0.0001). The wild-type strain produced a mucoviscous exopolysaccharide web, actively proliferated in nonimmune human serum, resisted phagocytosis, and caused liver microabscess and meningitis in mice. However, magA− mutants lost the exopolysaccharide web and became extremely serum sensitive, phagocytosis susceptible, and avirulent to mice. Virulence was restored by complementation using a magA-containing plasmid. We conclude that magA fits molecular Koch's postulates as a virulence gene. Thus, this locus can be used as a marker for the rapid diagnosis and for tracing the source of this emerging infectious disease.

scholarly journals Regulation of the Ysa Type III Secretion System of Yersinia enterocolitica by YsaE/SycB and YsrS/YsrR

2004 ◽  
Vol 186 (13) ◽  
pp. 4056-4066 ◽  
Author(s):  
Kimberly A. Walker ◽  
Virginia L. Miller
Keyword(s):  
Yersinia Enterocolitica ◽  
Type Iii Secretion ◽  
Shigella Flexneri ◽  
Wild Type ◽  
Secretion Systems ◽  
Type Iii ◽  
Regulatory Cascade ◽  
Two Component

ABSTRACT Yersinia enterocolitica biovar 1B contains two type III secretion systems (TTSSs), the plasmid-encoded Ysc-Yop system and the chromosomally encoded Ysa-Ysp system. Proteins secreted from the Ysa TTSS (Ysps) have only been detected in vitro when cells are cultured at 26°C in a high-NaCl medium. However, the exact role of the Ysa TTSS is unclear. Thus, investigations into the regulation of this system may help elucidate the role of the Ysps during the life cycle of Y. enterocolitica. Here we present evidence that the AraC-like regulator YsaE acts together with the chaperone SycB to regulate transcription of the sycByspBCDA operon, a phenomenon similar to that seen in the closely related Salmonella SPI-1 and Shigella flexneri Mxi-Spa-Ipa TTSSs. Deletion of either sycB or ysaE results in a twofold reduction in the activity of a sycB-lacZ fusion compared to the wild type. In a reconstituted Escherichia coli system, transcription of sycB was activated sixfold only when both YsaE and SycB were present, demonstrating that they are necessary for activation. ysrR and ysrS are located near the ysa genes and encode a putative two-component regulatory system. Mutations in either gene indicated that both YsrR and YsrS were required for secretion of Ysps. In addition, transcription from sycB-lacZ and ysaE-lacZ fusions was decreased 6.5- and 25-fold, respectively, in the ysrS mutant compared to the wild type. Furthermore, in the absence of NaCl, the activity of ysaE-lacZ was reduced 25-fold in the wild-type and ΔysrS strains, indicating that YsrS is probably required for the salt-dependent expression of the ysa locus. These results suggest that the putative two-component system YsrRS may be a key element in the regulatory cascade for the Ysa TTSS.

scholarly journals Plant Two-Component Signaling Systems and the Role of Response Regulators

2002 ◽  
Vol 128 (2) ◽  
pp. 363-369 ◽  
Author(s):  
Jens Lohrmann ◽  
Klaus Harter
Keyword(s):  
Response Regulators ◽  
Signaling Systems ◽  
Two Component

scholarly journals Modulation of Expression of the ToxR Regulon in Vibrio cholerae by a Member of the Two-Component Family of Response Regulators

1998 ◽  
Vol 66 (12) ◽  
pp. 5854-5861 ◽  
Author(s):  
Sandy M. Wong ◽  
Patricia A. Carroll ◽  
Laurence G. Rahme ◽  
Frederick M. Ausubel ◽  
Stephen B. Calderwood
Keyword(s):  
Gene Expression ◽  
Vibrio Cholerae ◽  
Virulence Factors ◽  
Bacterial Species ◽  
Virulence Gene ◽  
Response Regulators ◽  
Key Factors ◽  
Virulence Gene Expression ◽  
The Family ◽  
Two Component

ABSTRACT The ToxRS system in Vibrio cholerae plays a central role in the modulation of virulence gene expression in response to environmental stimuli. An integration of multiple signalling inputs mediated by ToxR, -S, and -T controls virulence gene expression leading to cholera toxin (CT) production. Recently, we identified a new virulence locus, varA (virulence associated regulator), in classical V. cholerae O1 that positively controls transcription of tcpA, the major subunit of the toxin-coregulated pilus (TCP) and the production of CT, two key factors in cholera pathogenesis. The varA locus is a homolog ofgacA (originally described for the soil organismPseudomonas fluorescens), which encodes a conserved global regulator belonging to the family of two-component signal transducing molecules. GacA homologs in a number of diverse gram-negative pathogenic bacterial species have been implicated in controlling the production of diverse virulence factors.varA mutants showed reduced levels of tcpAmessage and TcpA protein, lacked visible signs of autoagglutination (a phenotype associated with functional TCP), produced decreased levels of CT, and were attenuated in colonizing infant mice. Transcription ofvarA appears to be independent of ToxR, and overexpression of the regulators tcpPH and toxT from plasmids in the varA mutant restored wild-type levels of CT production and the ability to autoagglutinate. varArepresents an additional modulating factor in the coordinate expression of virulence factors in V. cholerae.

scholarly journals A novel PilR/PilS two-component system regulates NE pilus production in Clostridium perfringens

2021 ◽  
Author(s):  
Yuanyuan Zhou ◽  
Dion Lepp ◽  
Jason Carere ◽  
Hai Yu ◽  
Chengbo Yang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Clostridium Perfringens ◽  
Binding Activity ◽  
Necrotic Enteritis ◽  
Wild Type ◽  
Two Component System ◽  
Collagen Binding ◽  
Component System ◽  
Two Component

Clostridium perfringens causes necrotic enteritis (NE) in poultry. A chromosomal locus (VR-10B) was previously identified in NE-causing C. perfringens strains that encodes an adhesive pilus (NE pilus), along with a two-component system (TCS), designated here as PilRS. While the NE pilus is important in pathogenesis, the role of PilRS remains to be determined. The current study investigated the function of PilRS, as well as the Agr-like quorum-sensing (QS) system and VirSR TCS, in the regulation of pilin production. Isogenic pilR , agrB and virR null mutants were generated from parent strain CP1 by insertional inactivation using the ClosTron system, along with the respective complemented strains. Immunoblotting analyses showed no detectable pilus production in the CP1 pilR mutant, while production in its complement (CP1 pilR +) was greater than wild-type levels. In contrast, pilus production in the agrB and virR mutants was comparable or higher than the wild type, but reduced in their respective complemented strains. When examined for collagen-binding activity, the pilR mutant showed significantly lower binding to most collagen types (types I – V) than CP1 ( p ≤ 0.05), whereas this activity was restored in the complemented strain ( p > 0.05). In contrast, binding of agrB and virR mutants to collagen showed no significant differences in collagen-binding activity compared to CP1 ( p > 0.05), whereas the complemented strains exhibited significantly reduced binding ( p ≤ 0.05). These data suggest that the PilRS TCS positively regulates pilus production in C. perfringens , while the Agr-like QS system may serve as a negative regulator of this operon. Importance Clostridium perfringens type G isolates cause necrotic enteritis (NE) in poultry, presenting a major challenge for poultry production in the post-antibiotic era. Multiple factors in C. perfringens , including both virulent and non-virulent, are involved in the development of the disease. We previously discovered a cluster of C. perfringens genes that encode a pilus involved in adherence and NE development and a predicted two-component regulatory system (TCS), designated PilRS. In the present study, we have demonstrated the role of PilRS in regulating pilus production and collagen binding of C. perfringens . In addition, the Agr-like quorum sensing signalling pathway was found to be involved in the regulation. These findings have identified additional targets for developing non-antibiotic strategies to control NE disease.

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